Immunology Flashcards

1
Q

Define immunology

A

The study of the physiological mechanisms that we use to defend our bodies against invasion by other organism

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2
Q

Hypervariable regions

A

Antibodies have 3 and these determine the complementary fit between the antigen and the antigen binding site of the antibody

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3
Q

CDR’s

A

Complementary determining regions (part of the antibody and align with the loops at the end of the variable domain) which interact with the antigen and give the antibody specificity

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4
Q

Antigen binding

A

Bind to the antigen binding site of the antibody by non covalent forces (hydrogen, ionic, VDWs and hydrophobic)=weak bonds so a large number is required to ensure the 2 parts bind together

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5
Q

Antibody affinity

A

Strength of the total non-covalent interactions with a single antigen binding site on the antibody and a single epitope on the antigen

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6
Q

Antibody avidity

A

Overall strength of multiple interactions between an antibody with multiple antigen binding sites and a complex antigen with multiple epitopes

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7
Q

Antibody cross-reactivity

A

Antibody with an antigen binding site complementary to a specific antigen can also recognise different antigens with a similar structure

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8
Q

IgG

A
  • Gamma heavy chain
  • Must abundant immunoglobulin
  • Found in the blood and extracellular fluid
  • Variability of the heavy chain at the hinge region gives rise to 4 different subclasses which have subtly different functions
  • Activates the classical complement pathway
  • Can be actively transported across the placenta to give the foetus passive immunity and therefore protect it
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9
Q

IgA

A
  • alpha heavy chain
  • Variation of the heavy chain at the hinge region gives rise to 2 different subclasses which have subtly different functions
  • found in breast milk
  • multimeric due to formation of J chains, but IgA in the blood is monomeric
  • monomer in the blood and dimer in secretion
  • Secretion protects mucosal surfaces
  • Secretory component of antibody protects it from degradation
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10
Q

IgM

A
  • mu heavy chain
  • first immunoglobulin synthesised from infection in the primary immune response
  • 5 monomers joined and held together by J chains=multimeric
  • activates agglutination and the complement pathway
  • multiple binding sites allow for agglutination and to compensate for the low affinity
  • mainly found in the blood
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11
Q

IgE

A
  • epsilon heavy chain
  • produced to defend against parasitic infections and allergic reactions
  • binds to the high affinity Fc receptors on the mast cells and basophils which are complementary to this specific antibody
  • the cross linking by antigen triggers the mast cell activation, degranulation and hence histamine and other inflammatory mediator release
  • found at low concentrations/levels within the blood serum
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12
Q

IgD

A
  • sigma heavy chain
  • very low blood serum concentration
  • Involved in the B cell development and activation
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13
Q

Light chains

A

Can be either both kappa or both lambda (cannot be one of each because the antibody molecule is symmetrical)

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14
Q

Antibody roles

A

Roles in medicine, laboratory science and in defence

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15
Q

Laboratory science antibody roles

A

vast range of diagnostic and research applications

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16
Q

Medicine antibody roles

A
  • Monoclonal antibody therapy for cancer treatment
  • Antibody levels can help diagnose disease and monitor disease progress
  • Pooled antibodies for passive immunity/therapy
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17
Q

Defence antibody roles

A
  • Neutralisation of toxins by antibodies binding to antigens/toxin molecules
  • Passive immunity in newborns with the antibodies gained from the mother
  • Opsonisation=coating of the pathogens with antibodies (proteins) to promote phagocytosis, aiding the phagocytes
  • Agglutination=antibodies can clump the pathogens together due to their multiple antigen binding sites
  • Complement activation via the classical pathway
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18
Q

Where are the B cells produced and mature?

A

Produced by haematopoietic stem cells in the bone marrow and mature here also before being released into the bloodstream/circulation as naïve B lymphocytes

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19
Q

Role of B lymphocytes

A

Occur in humoral immunity and if complementary antigen to binding site is encountered, cell proliferation occurs by clonal selection and antibodies of the same specificity will be synthesised

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20
Q

Antigen epitope

A

The specific part of the antigen to which the receptor binds. Antigens have multiple epitopes so a single antigen can be targeted by multiple antibodies

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21
Q

B cell receptor

A

Membrane bound antibody which binds to the epitope of antigens. Also consists of a di-sulfate linked heterodimer with an IgA and IgB component

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22
Q

Di-sulfate linked heterodimer

A

Cytoplasmic tail is long enough to interact with the intracellular components and trigger a cascade

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23
Q

Immunoglobulin gene rearrangement

A
  • Accounts for multiple B cell receptors
  • Occurs in bone marrow when progenitor B cells are converted to mature B cells
  • Immature B cells begin with germline DNA
  • Heavy chain has 3 gene segments=V,D and J regions
  • Regions are composed of many segments and a singular segment is selected from each region to join to the constant region
  • VDJ regions formed from recombination with addition/removal of DNA, then transcription and splicing
  • light chain is V and J=no D
  • 3 enzymes involved=kappa, lambda, all heavy
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24
Q

VDJ recombinase

A

Discards unwanted loops of DNA

-Includes enzymes RAG 1 and RAG 2

25
Q

Alternative RNA splicing

A

IgD and IgM are co-expressed

26
Q

Plasma B cell

A

produces antibodies

-requires an accessory signal from microbial constituents or activation from a T cell

27
Q

Memory B cell

A

prepares for future infections=subsequent infections with the same antigen

28
Q

Somatic hypermutation and affinity maturation

A

improves antibody quality

29
Q

IgM BCRs

A

only immunoglobulin receptor which can recognise PAMPs

30
Q

Activation by T helper cells

A
  • Antigen binds to BCR and is internalised by B cell
  • degraded into peptides on presented on membrane via MHC class 2 receptors
  • dendritic cell also has antigen presented in MHC class 2
  • dendritic antigen recognised by CD4 T helper cell
  • T cell migrates to lymph nodes and encounters B cell with the same antigen=activates
  • B cell proliferates and divides
31
Q

Ig class switching

A
  • Gene segment rearrangement in the constant region

- Secreted cytokines switches class

32
Q

Somatic hypermutation and affinity maturation

A
  • more specialised BCR
  • once bound to antigen, AID enzyme alters variable region in B cell DNA=introducing point mutations to AT
  • Point mutations change the antibody structure helping the antibody bind more strongly to the antigen
  • weaker binding antibodies are selected against and don’t survive
  • leads to improvement of antibody quality
33
Q

Primary antibody response

A

Involves IgM=not very protective

34
Q

Secondary antibody response

A

Class switch so memory cells change from IgM to IgG

35
Q

Cytokines

A
  • secreted by immune cells

- small secreted proteins

36
Q

Type 1 interferons

A

Activates natural killers and anti viral defence

37
Q

Type 2 interferons

A

Produced by T cells usually and proinflammatory

38
Q

Pre-infection body defences

A

Mechanical, chemical and microbiological

39
Q

Cytokine storm

A

Overproduction of cytokines leading to accumulation of immune system cells=can lead to death

40
Q

Defence against bacteria

A
  • Surface defences
  • fever
  • phagocytosis
  • antibody opsonisation
  • complement activation via the alternative pathway
  • release of inflammatory mediators and acute phase proteins
41
Q

Defence against viruses

A

-surface defences
-interferons
-Natural killer cells
-release of inflammatory mediators and acute phase proteins
-T cells mainly resolving infection
antibody, complement, ADCC

42
Q

Gram positive

A

Violet, 1 cytoplasmic membrane, staph aureus not e coli (gram negative)

43
Q

Immune system function

A

Prevent infections by non self molecules

  • too much=immune hyper-activation autoimmunity
  • too little=infections
44
Q

Pathogen recognition

A
  • bacteria enter body
  • PRR’s recognise PAMPs
  • trigger innate response
  • APC’s process and present antigen peptides to adaptive immunity
45
Q

MHC class 2

A
  • APC’s

- presents exogenous peptides on CD4 helper T cells

46
Q

MHC class 1

A
  • all nucleated cells

- endogenous peptides on CD8 cytotoxic T cells

47
Q

MHC

A
  • highly polymorphic

- presents processed antigens to T lymphocytes

48
Q

MHC class 2

A

heterodimer of 2 alpha 2 beta

49
Q

MHC class 1

A

heterodimer of 3 alpha 1 beta microglobulin

50
Q

cytotoxic

A
  • direct killing
  • membrane perforation
  • fas to fasL induced apoptosis
51
Q

T cell pathway

A
  • precursor in bone marrow
  • mature with markers in thymus
  • gene rearrangement in cortex and survival of T cells with useful TCR which binds to antigens
  • medulla sees elimination of T cells which bind too strongly to MHC
  • MHC bound peptide then co-stimulation then cytokine stimulation
52
Q

Helper

A
  • response modulation
  • secrete cytokines
  • recruit other immune cells
53
Q

Cytotoxic T cells

A

-virally infected or transformed cells

54
Q

Th1

A

intracellular infection=macrophage activation

55
Q

Th2

A

allergy

56
Q

Th17

A

inflammation, bacterial and fungal infection

57
Q

Treg

A
  • regulation of effector T cell function=regulation of immune response
  • switch off naïve or activated effector T cells
  • anergy (absence of normal immune response), deletion or regulation
  • regulation=T cell not exposed to the antigen or there is insufficient amount of antigen to activate it
58
Q

Role of Treg

A

-prevents excessive tissue damage (healthy tissue damage)

59
Q

Lymphocytes

A
  • regulation by cytokines
  • prevent responses against self. central tolerance (thymus) and peripheral tolerance (anergy, deletion, regulation and ignorance) and prevents responses to also avoid tissue damage (lymphocytes apoptose after infection is cleared)